目的

探讨中度颅脑液压损伤(TBI)大鼠模型生化指标脂质氧化终产物丙二醛(MDA)及抗氧化剂谷胱甘肽(GSH)含量相关指标的变化，并探讨其与继发性脑损伤间的关系。

方法

将雄性Sprague-Dawley 大鼠48 只按随机数字表法分成中度颅脑损伤(mTBI)组和假手术(Sham-TBI)组，每组24 只。以液压中度TBI 指标致伤mTBI 组，并于伤后6 h、24 h 处死大鼠，通过ELISA免疫酶技术测定抗氧化剂GSH和脂质氧化产物MDA在2组的不同表达，评价大鼠颅脑创伤后的氧化应激损伤。应用SPSS 19.0统计软件，对两组的GSH和MDA浓度比较采用独立样本t检验。

结果

mTBI组脑组织见挫伤灶及蛛网膜下腔出血，HE染色后可见神经元损伤核固缩，细胞坏死呈空泡状，而Sham-TBI 组未见神经元损伤表现。TBI 后mTBI 组中的MDA 浓度较Sham-TBI 组显著升高[6 h 时分别为(8.34±2.03)μg/g 和(3.92±1.20)μg/g，t=6.493，P=0.000]，随伤后时间的延长，MDA 的浓度显著升高[24 h 时分别为(12.74±2.44)μg/g 和(3.96±1.18)μg/g，t=11.222，P=0.000]；而TBI 后mTBI 组GSH 浓度显著低于Sham-TBI 组[6 h 时分别为(2.65±0.63)μg/g 和(4.90±0.56)μg/g，t=9.247，P=0.000]，随伤后时间的延长，GSH 的浓度显著降低[24 h 时分别为(2.20±0.62)μg/g 和(4.88±0.55)μg/g；t=11.202，P=0.000]。

结论

液压TBI 模型致伤能量能够测量，中度闭合性颅脑外伤可导致脑组织病理学改变和氧化应激损伤，且氧化应激损伤指标与脑损伤时间呈正相关，外伤后早期阻断氧化应激过程可能起到脑保护作用。

Objective

To study the change of biochemical index of malondialdehyde (MDA)and glutathione(GSH)of moderate traumatic brain injury(TBI)rats model,which are the end products of lipid oxidation and antioxidant, respectively. To explore the relationship between these two chemicals and secondary brain injury.

Methods

48 adult male Sprague-Dawley rats were randomly assigned to 2 groups : moderate-TBI (mTBI, n=24) group and sham-TBI (sham, n=24) group.Hydraulic moderate TBI index was induced to mTBI group. The rats were killed 6 h and 24 h after injured respectively, the levels of MDA and GSH were examined by ELISA enzymictechnology to analyze the different expression among 2 groups and to evaluate the oxidative stress injury of the rats after traumatic brain injury. The data was analyzed by SPSS 19.0 statistical analysis software, the concentration of GSH and MDA among 2 groups was tested by independent-samples t Test.

Results

Brain contusion and subarachnoid hemorrhage could be observed in mTBI rats, in brain sections with HE staining, nuclear pyknosis and vesicular neurons could be detected. However, no similar injury could be found in sham group.The concentration of MDA in mTBI group was significantly higher than that in sham group (in 6 h, level of mTBI 8.34±2.03μg/g, level of sham 3.92±1.20μg/g, t=6.493,P=0.000), and the concentration displayed a significant upregulated trend as time went by post TBI (in 24 h, level of mTBI 12.74±2.44μg/g, level of sham 3.96±1.18μg/g, t=11.222, P=0.000). The concentration of GSH in mTBI group was significantly lower than that in sham group (in 6 h, level of mTBI 2.65±0.63μg/g, level of sham 4.90±0.56μg/g, t=9.247, P=0.000), and the concentration displayed a significant downtrend as time went by post TBI (in 24 h, level of mTBI 2.20±0.62μg/g,level of sham 4.88±0.55μg/g, t=11.202, P=0.000).

Conclusions

The injury level of hydraulic TBI model can be evaluated,moderate closed brain trauma resulted in brain tissue pathological changes and oxidative stress injury.The index of oxidative stress was correlated with the injury period.Blockage of the process of the oxidative stress in the early stage post TBI may play an important role in neuroprotective effect.